The invention generally relates to cardiac pacing techniques and in particular to techniques for treating vasovagal syncope using cardiac pacing.
Syncope is a sudden loss of strength or consciousness caused by reduced cerebral circulation, itself typically the result of vasodilation. Vasovagal syncope is a type of syncope referred to as a neurocardiogenic syncope wherein the syncope is triggered by an interaction between the heart and nerve tissue connected to the heart. Neurocardiogenic syncope may also be referred to as neuromediated syncope, neurally mediated syncope, neurocardiogenic syncope, cardioneurogenic syncope, vasodepressor syncope, malignant vasovagal syndrome, neurally mediated hypotension/bradycardia and cardiovascular neurogenic syncope. For vasovagal syncope, the interaction occurs between the heart and the vagus nerve.
Evidence suggests that vasovagal syncope is initially triggered by a sudden reduction in peripheral vascular resistance, perhaps resulting from stress, pooling of blood in the extremities, or other factors. As a result of the reduction in peripheral vascular resistance, the pressure of blood entering the heart drops and the amount of blood filling the ventricles prior to ventricular contractions therefore also drops. With less blood in the ventricles, the ventricles thereby contract much more quickly and vigorously than would otherwise occur in an effort to maintain a constant stroke volume. The more vigorous ventricular contractions have the effect of stimulating ventricular mechanoreceptors, also known as C fibers, that normally only respond to ventricular expansion or stretching, rather than contraction. The activation of the ventricular mechanoreceptors results in a surge in neural traffic to the brainstem, particularly to the nucleus tractus solitaries, via the vasovagal nerve.
For most people, the neurological system properly interprets the increase of activity of the mechanoreceptors as being in response to a drop in peripheral vascular resistance and compensates by increasing the heart rate and constricting the blood vessels. However, in certain patients, as a result of a neurological condition within the vagus nerve or for some other reason, the surge in neural traffic is falsely perceived by the neurological system as being representative of hypertension. In response thereto, the brainstem triggers an increase in peripheral vasodilation and a reduction in heart rate. The vasodilation and the drop in heart rate, in turn, cause a still further reduction in blood pressure, i.e., hypotension. In other words, the actions taken by the brainstem exacerbate the problem. If the degree of hypotension is sufficiently severe, cerebral hypoperfusion occurs wherein brain cells do not receive enough oxygen and, consequently, the victim loses consciousness. Accordingly, within these patients, any sudden drop in peripheral vascular resistance can trigger vasovagal syncope and the patients then suffer from recurrent vasovagal syncope. Further information regarding vasovagal syncope may be found in S. Serge Barold and Jacques Mugica, Recent Advances in Cardiac Pacing, Futura Publishing Company, 92-95, 1997.
As can be appreciated, loss of consciousness can be particularly dangerous for the patient if occurring while the patient is driving a motor vehicle, climbing a flight of stairs or engaged in any other activity wherein the loss of consciousness could result in injury or death. Accordingly, it is highly desirable to provide techniques for preventing or at least mitigating the symptoms that occur from vasovagal syncope or other forms of neurocardiological syncope.
One possible technique for preventing vasovagal syncope is to employ a pacemaker, or other implantable cardiac pacing device, to pace the heart to prevent the reduction in blood pressure associated with vasovagal syncope from occurring. Indeed, the American College of Cardiology-American Heart Association suggested in 1991 that vasovagal syncope in patients should be used as a Class 2 indication for pacing therapy. However, conventional cardiac pacemakers have had only limited success in preventing recurrent vasovagal syncope. (See David G. Benditt et al., Cardiac Pacing for Prevention of Recurrent Vasovagal Syncope, Ann Intem Med. 1995; 122; 204-209.) Insofar as vasovagal syncope is concerned, conventional pacemakers only respond to the reduction in heart rate associated therewith. The reduction in heart rate, also referred to as bradycardia, is detected by the pacemaker, which increases the heart rate to compensate. Depending upon the programming of the pacemaker, it may take five to eight seconds or more before the pacemaker begins increasing the heart rate in response to detection of bradycardia. For many patients subject to recurrent vasovagal syncope, a significant drop in blood pressure occurs before there is any bradycardia. Hence, by the time the pacemaker begins to increase the heart rate, the blood pressure will already have dropped to the point where the increase in heart rate is ineffective. In this regard, the drop in blood pressure results in significantly less blood filling the ventricles, such that there is simply not enough incoming blood to pump. Hence, overall blood pressure is not significantly increased merely by pumping the heart faster, and the aforementioned cerebral hypoperfusion still occurs resulting in unconsciousness. Moreover, for at least some patients subject to recurrent vasovagal syncope, there is no significant drop in heart rate, only a drop in blood pressure. Hence, pacemakers programmed to prevent vasovagal syncope based solely upon detection of bradycardia will have little or no effect.
Thus, bradycardia-triggered vasovagal syncope prevention techniques employed by some conventional cardiac pacemakers often fail to prevent the syncope. Moreover, conventional cardiac pacemakers are often unable to distinguish physiologic bradycardia such as that associated with sleep from bradycardia associated with vasovagal syncope or other neurocardiogenic syncope.
Accordingly, it would be highly desirable to provide improved cardiac pacing devices capable of predicting the onset of vasovagal syncope or other types of neurocardiogenic syncope, and for reliably administering pacing therapy to prevent the syncope from occurring. It is to these ends that the invention is primarily directed.
In accordance with one aspect of the invention, a cardiac pacing device is provided with a control system that is programmed or configured to execute vasovagal syncope prediction, compensation, and/or prevention algorithms for predicting the onset of vasovagal syncope and for administering pacing therapy to prevent the syncope from occurring or at least mitigate symptoms related to vasovagal syncope. That is, an increase in pacing rate can be used to compensate for the decrease in cardiac output associated vasovagal syncope that occur with pathological changes in vagal tone. Prediction of the onset of vasovagal syncope is based upon an analysis of the contractility of the heart muscle.
In an exemplary embodiment, prediction of the onset of vasovagal syncope is achieved by sensing the contractility of the heart muscle and determining whether the sensed contractility exceeds an average contractility by a predetermined threshold amount. If so, the heart is paced at a xe2x80x9cvasovagal syncope prevention ratexe2x80x9d, which may be, for example, 20 to 40 beats per minute faster than a previous heart rate. Hereinafter, the term xe2x80x9cvasovagal syncope prevention ratexe2x80x9d is understood to mean a rate that prevents or mitigates the symptoms related to vasovagal syncope. The term xe2x80x9cpreventative pacingxe2x80x9d, as used herein, is also understood to include preventing or compensating for an episode of vasovagal syncope, including episodes of sudden rate drop and vasodilation that result in poor or sudden decreases in vagal tone, which are compensated by increasing cardiac output with an increase in pacing rate.
In one embodiment, the contractility of the heart is determined, for example, by measuring the electrical impedance change or pressure change in the ventricle, or by measuring the movement of heart tissue in the wall of the heart using an accelerometer. The contractility measured is averaged over a period of time to determine the average contractility.
It is recognized that the contractility of the heart may be determined in a variety of ways, as will be shown below. Since the exact method is not critical to practicing the invention, it is within the spirit of the invention that any method of determining contractility may be employed. However, for convenience and simplicity, it is preferred to employ a technique that does not require a special lead, for example, by measuring the electrical impedance or the rate of change of impedance, ventricular gradient or post-depolarization integral, QT interval, heart sounds, etc. Specially-made leads that incorporate sensors, of course, may also be used, for example, leads that measure pressure change in the ventricle, or by measuring the movement of heart tissue in the wall of the heart using an accelerometer. In any case, the contractility measured is averaged over a period of time to determine the average contractility.
In this manner, the onset of vasovagal syncope is predicted based upon changes in heart muscle contractility and syncope is substantially prevented from occurring, or at least the symptoms are mitigated, by immediately administering vasovagal syncope preventative pacing measures. Because prediction of imminent vasovagal syncope is based upon a measurement of the contractility of the heart tissue, rather than upon detection of an episode of bradycardia, vasovagal syncope is thereby detected even in circumstances wherein hypotension occurs before bradycardia or wherein bradycardia does not occur at all. Also, physiologic episodes of bradycardia, such as those associated with sleep, do not erroneously trigger the vasovagal syncope pacing therapy. Moreover, the increase in contractility associated with vasovagal syncope can be detected quickly whereas reliable bradycardia detection may require analysis of several heart beats. Hence, preventative pacing may be administered before the blood pressure has dropped significantly, as could otherwise occur if relying solely on bradycardia detection. Two or more independent contractility sensors may be provided to help prevent a false positive detection of vasovagal syncope.
Method embodiments of the invention are also provided. Other features, advantages and aspects of the invention are either described below or will be apparent from the descriptions below in combination with the accompanying drawings.